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Resveratrol reduces brain injury after subarachnoid hemorrhage by inhibiting oxidative stress and endoplasmic reticulum stress

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Neural Regeneration Research 2019年第10期14卷 1734-1742页

作者： Yun-Kai Xie Xin Zhou Hong-Tao Yuan Jie Qiu Dan-Qing Xin Xi-Li Chu Da-Chuan Wang Zhen Wang Department of Physiology School of Basic Medical SciencesShandong UniversityJinanShandong ProvinceChina Department of Spinal Surgery Shandong Provincial Hospital Affiliated to Shandong UniversityJinanShandong ProvinceChina

Previous studies have shown that resveratrol,a bioactive substance found in many plants,can reduce early brain injury after subarachnoid hemorrhage,but how it acts is still unclear.This study explored the mechanism using the experimental subarachnoid hemorrhage rat model established by injecting autologous blood into the cerebellomedullary cistern.Rat models were treated with an intraperitoneal injection of 60 mg/kg resveratrol 2,6,24 and 46 hours after injury.At 48 hours after injury,their neurological function was assessed using a modified Garcia score.Brain edema was measured by the wet-dry method.Neuronal apoptosis in the prefrontal cortex was detected by terminal deoxyribonucleotidyl transferase-mediated biotin-16-dUTP nick-end labeling assay.Levels of reactive oxygen species and malondialdehyde in the prefrontal cortex were determined by colorimetry.CHOP,glucose-regulated protein 78,nuclear factor-erythroid2-related factor 2 and heme oxygenase-1 mRNA expression levels in the prefrontal cortex were measured by reverse transcription polymerase chain reaction.Tumor necrosis factor-alpha content in the prefrontal cortex was detected by enzyme linked immunosorbent assay.Immunohistochemical staining was used to detect the number of positive cells of nuclear factor-erythroid 2-related factor 2,heme oxygenase 1,glucose-regulated protein 78,CHOP and glial fibrillary acidic protein.Western blot assay was utilized to analyze the expression levels of nuclear factor-erythroid 2-related factor 2,heme oxygenase 1,glucose-regulated protein 78 and CHOP protein expression levels in the prefrontal cortex.The results showed that resveratrol treatment markedly alleviated neurological deficits and brain edema in experimental subarachnoid hemorrhage rats,and reduced neuronal apoptosis in the prefrontal cortex.Resveratrol reduced the levels of reactive oxygen species and malondialdehyde,and increased the expression of nuclear factor-erythroid 2-related factor 2,heme oxygenase-1 mRNA and protein in the prefrontal cortex.Resveratrol

关键词： nerve regeneration resveratrol oxidative stress endoplasmic reticulum stress neuroinflammation subarachnoid hemorrhage nuclear factor-erythroid 2-related factor 2 heme oxygenase-1 glucose-regulated protein 78 neural regeneration

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Potential therapeutic molecular targets for blood-brain barrier disruption after subarachnoid hemorrhage

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Neural Regeneration Research 2019年第7期14卷 1138-1143页

作者： Hideki Kanamaru Hidenori Suzuki Department of Neurosurgery Mie University Graduate School of Medicine

Aneurysmal subarachnoid hemorrhage remains serious hemorrhagic stroke with high morbidities and mortalities.Aneurysm rupture causes arterial bleeding-induced mechanical brain tissue injuries and elevated intracranial pressure,followed by global cerebral ischemia.Post-subarachnoid hemorrhage ischemia,tissue injuries as well as extravasated blood components and the breakdown products activate microglia,astrocytes and Toll-like receptor 4,and disrupt blood-brain barrier associated with the induction of many inflammatory and other cascades.Once blood-brain barrier is disrupted,brain tissues are directly exposed to harmful blood contents and immune cells,which aggravate brain injuries furthermore.Blood-brain barrier disruption after subarachnoid hemorrhage may be developed by a variety of mechanisms including endothelial cell apoptosis and disruption of tight junction proteins.Many molecules and pathways have been reported to disrupt the blood-brain barrier after subarachnoid hemorrhage,but the exact mechanisms remain unclear.Multiple independent and/or interconnected signaling pathways may be involved in blood-brain barrier disruption after subarachnoid hemorrhage.This review provides recent understandings of the mechanisms and the potential therapeutic targets of blood-brain barrier disruption after subarachnoid hemorrhage.

关键词： blood-brain barrier early brain injury endothelial cell subarachnoid hemorrhage tight junction inflammation matricellular protein Toll-like receptor 4 TLR4

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Stent-grafts placement for treatment of massive hemorrhage from ruptured hepatic artery after pancreaticoduodenectomy

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World Journal of Gastroenterology 2010年第29期16卷 3716-3722页

作者： Mao-Qiang Wang Feng-Yong Liu Feng Duan Zhi-Jun Wang Peng Song Qing-Sheng Fan Department of Interventional Radiology Chinese PLA General HospitalBeijing 100853China

AIM:To present a series of cases with life-threatening hemorrhage from ruptured hepatic artery pseudoaneurysm after pancreaticoduodenectomy(PD) treated with placement of stent-grafts.METHODS:Massive hemorrhage from ruptured hepatic artery pseudoaneurysm after PD in 9 patients(6 men,3 women) at the age of 23-75 years(mean 48 years),were treated with placement of percutaneous endovascular balloon-expandable coronary stent-grafts.All patients were not suitable for embolization because of a non-patent portal vein.One or more stent-grafts,ranging 3-6 mm in diameter and 16-55 mm in length,were placed to exclude ruptured pseudoaneurysm.Followup data,including clinical condition,liver function tests,and Doppler ultrasound examination,were recorded at the outpatient clinic.RESULTS:Immediate technical success was achieved in all the 9 patients.All stent-grafts were deployed in the intended position for immediate cessation of bleeding and preservation of satisfactory hepatic arterial blood flow.No significant procedure-related complications occurred.Recurrent bleeding occurred in 2 patients at 16 and 24 h,respectively,after placement of stent-grafts and treated with surgical revision.One patient died of sepsis 12 d after the interventional procedure.The remaining 6 patients were survived when they were discharged.The mean follow-up time was 10.5 mo(range 4-16 mo).No patient had recurrent bleeding after discharge.Doppler ultrasound examination verified the patency of hepatic artery and stent-grafts during the follow-up.CONCLUSION:Placement of stent-grafts is an effective and safe procedure for acute life-threatening hemorrhage from ruptured hepatic artery pseudoaneurysm.

关键词： Pancreaticoduodenectomy hemorrhage Hepatic artery Pseudoaneurysm Stent-graft

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Neuroprotection mediated by the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage

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Neural Regeneration Research 2019年第6期14卷 1013-1024页

作者： Yang Wang De-Jun Bao Bin Xu Chuan-Dong Cheng Yong-Fei Dong Xiang-pin Wei Chao-Shi Niu Department of Neurosurgery First Affiliated Hospital of USTCDivision of Life Sciences and MedicineUniversity of Science and Technology of China Anhui Medical University Auhui Province Medical Genetic Center Anhui Province Key Laboratory of Brain Function and Brain Disease

The Wnt/Frizzled signaling pathway participates in many inflammation-linked diseases. However, the inflammatory response mediated by the Wnt/Frizzled signaling pathway in experimental subarachnoid hemorrhage has not been thoroughly investigated. Consequently, in this study, we examined the potential role of the Wnt/Frizzled signaling pathway in early brain injury in rat models of subarachnoid hemorrhage.Simultaneously, possible neuroprotective mechanisms were also investigated. Experimental subarachnoid hemorrhage rat models were induced by injecting autologous blood into the prechiasmatic cistern. Experiment 1 was designed to examine expression of the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage. In total, 42 adult rats were divided into sham(injection of equivalent volume of saline), 6-, 12-, 24-, 48-, 72-hour, and 1-week subarachnoid hemorrhage groups. Experiment 2 was designed to examine neuroprotective mechanisms of the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage. Rats were treated with recombinant human Wnt1(rhwnt1), small interfering Wnt1(siwnt1) RNA, and monoclonal antibody of Frizzled1(anti-Frizzled1) at 48 hours after subarachnoid hemorrhage. Expression levels of Wnt1, Frizzled1, β-catenin, peroxisome proliferator-activated receptor-γ, CD36, and active nuclear factor-κB were examined by western blot assay and immunofluorescence staining. Microglia type conversion and inflammatory cytokine levels in brain tissue were examined by immunofluorescence staining and enzyme-linked immunosorbent assay. Our results show that compared with the sham group, expression levels of Wnt1, Frizzled1, and β-catenin were low and reduced to a minimum at 48 hours, gradually returning to baseline at 1 week after subarachnoid hemorrhage. rhwnt1 treatment markedly increased Wnt1 expression and alleviated subarachnoid hemorrhage-induced early brain injury(within 72 hours), including cortical cell apoptosis, brain edema, and neurobehavioral defi

关键词： nerve regeneration subarachnoid hemorrhage Wnt/Frizzled signaling pathway early brain injury nuclear factor-κB M2 type microglia peroxisome proliferator-activated receptor-γ inflammatory cytokines neural regeneration

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Magnesium:pathophysiological mechanisms and potential therapeutic roles in intracerebral hemorrhage

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Neural Regeneration Research 2019年第7期14卷 1116-1121页

作者： Jason J.Chang Rocco Armonda Nitin Goyal Adam S.Arthur Department of Critical Care Medicine MedStar Washington Hospital Center Department of Neurology Georgetown University School of Medicine Department of Neurosurgery Georgetown University School of Medicine Department of Neurology University of Tennessee Health Science Center Semmes Murphey Clinic Department of Neurosurgery University of Tennessee Health Science Center

Intracerebral hemorrhage(ICH) remains the second-most common form of stroke with high morbidity and mortality.ICH can be divided into two pathophysiological stages:an acute primary phase,including hematoma volume expansion,and a subacute secondary phase consisting of blood-brain barrier disruption and perihematomal edema expansion.To date,all major trials for ICH have targeted the primary phase with therapies designed to reduce hematoma expansion through blood pressure control,surgical evacuation,and hemostasis.However,none of these trials has resulted in improved clinical outcomes.Magnesium is a ubiquitous element that also plays roles in vasodilation,hemostasis,and blood-brain barrier preservation.Animal models have highlighted potential therapeutic roles for magnesium in neurological diseases specifically targeting these pathophysiological mechanisms.Retrospective studies have also demonstrated inverse associations between admission magnesium levels and hematoma volume,hematoma expansion,and clinical outcome in patients with ICH.These associations,coupled with the multifactorial role of magnesium that targets both primary and secondary phases of ICH,suggest that magnesium may be a viable target of study in future ICH studies.

关键词： intracerebral hemorrhage stroke,magnesium vasodilation hemostasis blood-brain barrier perihematomal edema

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Inducible heat shock protein 70 kD and inducible nitric oxide synthase in hemorrhage/resuscitation-induced injury

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Cell Research 2004年第6期14卷 450-459页

作者： Juliann G.KIANG Department of Cellular Injury Walter Reed Army Institute of Research Silver Spring MD 20910-7500 USA. Departments of Medicine and of Pharmacology Uniformed Services University of The Health Sciences Bethesda MD 20814-4799

Inducible heat shock protein 70 kD (HSP-70i) has been shown to protect cells, tissues, and organs from harmful assaults in in vivo and in vitro experimental models. Hemorrhagic shock followed by resuscitation is the principal cause of death among trauma patients and soldiers in the battlefield. Although the underlying mechanisms are still not fully understood, it has been shown that nitric oxide (NO) overproduction and inducible nitric oxide synthase (iNOS) over expression play important roles in producing injury caused by hemorrhagic shock including increases in polymorpho nuclear neutrophils (PMN) infiltration to injured tissues and leukotriene B4 (LTB4) generation. Moreover, transcription factors responsible for iNOS expression are also altered by hemorrhage and resuscitation. It has been evident that either up-regulation of HSP-70i or down-regulation of iNOS can limit tissue injury caused by ischemia/reperfusion or hemorrhage/resuscitation. In our laboratory, geldanamycin, a member of ansamycin famil

关键词： inducible HSP-70 iNOS eNOS hemorrhage caspase-3 ATP KLF6 resuscitation

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Imbalance of matrix metalloproteinase-9 and matrix metalloproteinase tissue inhibitor-1 may contribute to hemorrhage in cerebellar arteriovenous malformations

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Neural Regeneration Research 2012年第19期7卷 1513-1519页

作者： Fei Di Tongyan Chen Hongli Li Jizong Zhao Shuo Wang Yuanli Zhao Dong Zhang Department of Neurosurgery Beijing Tiantan Hospital Capital Medical University Beijing 100050 China Department of Laboratory Medicine Beijing Tiantan Hospital Capital Medical University Beijing 100050 China Department of Pathology Beijing Tiantan Hospital Capital Medical University Beijing 100050 China

In this study, we determined the expression levels of matrix metalloproteinase-2 and -9 and matrix metalloproteinase tissue inhibitor-1 and -2 in brain tissues and blood plasma of patients undergoing surgery for cerebellar arteriovenous malformations or primary epilepsy （control group）. Immunohistochemistry and enzyme-linked immunosorbent assay revealed that the expression of matrix metalloproteinase-9 and matrix metalloproteinase tissue inhibitor-1 was significantly higher in patients with cerebellar arteriovenous malformations than in patients with primary epilepsy. The ratio of matrix metalloproteinase-9 to matrix metalloproteinase tissue inhibitor-1 was significantly higher in patients with hemorrhagic cerebellar arteriovenous malformations compared with those with non-hemorrhagic malformations. Matrix metalloproteinase-2 and matrix metalloproteinase tissue inhibitor-2 levels were not significantly changed. These findings indicate that an imbalance of matrix metalloproteinase-9 and matrix metalloproteinase tissue inhibitor-I, resulting in a relative overabundance of matrix metalloproteinase-9, might be the underlying mechanism of hemorrhage of cerebellar arteriovenous malformations.

关键词： cerebellar arteriovenous malformations hemorrhage matrix metalloproteinase-2 matrixmetalloproteinase-9 tissue matrix metalloproteinase inhibitor-1 tissue matrix metalloproteinaseinhibitor-2 immunohistochemistry enzyme-linked immunosorbent assay neural regeneration

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Risk factors for delayed hemorrhage after endoscopic sphincterotomy

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Hepatobiliary & Pancreatic Diseases International 2020年第5期19卷 467-472页

作者： Jing Yan Chun-Xia Zhou Chong Wang Yuan-Yuan Li Le-Ying Yang You-Xiang Chen Jian-Jian Hu Guo-Hua Li Department of Gastroenterology The First Affiliated Hospital of Nanchang UniversityNanchang 330006China Department of Urology The First Affiliated Hospital of Nanchang UniversityNanchang 330006China

Background:hemorrhage is one of the most serious complications of endoscopic sphincterotomy(EST).The risk factors for delayed hemorrhage are not clear.This study aimed to explore the risk factors for post-EST delayed hemorrhage and suggest some precautionary measures.Methods:This study analyzed 8477 patients who successfully underwent endoscopic retrograde cholangiopancreatography(ERCP)and EST between January 2007 and June 2015 in the First Affiliated Hospital of Nanchang University.Univariate and multivariate analyses were performed to find the risk factors for delayed hemorrhage after EST.Results:Of the 8477 patients screened,137(1.62%)experienced delayed hemorrhage.Univariate analysis showed that male,the severity of jaundice,duodenal papillary adenoma and carcinoma,diabetes,intraoperative bleeding,moderate and large incisions,and directional deviation of incision were risk factors for post-EST delayed hemorrhage(Phemorrhage.Conclusions:Delayed hemorrhage is the most common and dangerous complication of EST.Intraoperative bleeding and directional deviation of incision are independent risk factors for post-EST delayed hemorrhage.

关键词： Endoscopic sphincterotomy Endoscopic retrograde cholangiopancreatography hemorrhage Risk factors

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Vascular endothelial growth factor A promotes platelet adhesion to collagen Ⅳ and causes early brain injury after subarachnoid hemorrhage

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Neural Regeneration Research 2019年第10期14卷 1726-1733页

作者： Zun-Wei Liu Jun-Jie Zhao Hong-Gang Pang Jin-Ning Song Department of Renal Transplantation Nephropathy Hospitalthe First Affiliated HospitalMedical College of Xi’an Jiaotong UniversityXi’anShaanxi ProvinceChina Institute of Organ Transplantation Xi’an Jiaotong UniversityXi’anShaanxi ProvinceChina Department of Neurosurgery the First Affiliated HospitalMedical College of Xi’an Jiaotong UniversityXi’anShaanxi ProvinceChina The First Affiliated Hospital Medical College of Xi’an Jiaotong UniversityXi’anShaanxi ProvinceChina

The role of vascular endothelial growth factor A in platelet adhesion in cerebral microvessels in the early stage of subarachnoid hemorrhage remains unclear.In this study,the endovascular puncture method was used to produce a rat model of subarachnoid hemorrhage.Then,30 minutes later,vascular endothelial growth factor A antagonist anti-vascular endothelial growth factor receptor 2 antibody,10μg,was injected into the right ventricle.Immunohistochemistry and western blot assay were used to assess expression of vascular endothelial growth factor A,occludin and claudin-5.Immunohistochemical double labeling was conducted to examine co-expression of GP Ⅰa-Ⅱ integrin and type Ⅳ collagen.TUNEL was used to detect apoptosis in the hippocampus.Neurological score was used to assess behavioral performance.After subarachnoid hemorrhage,the expression of vascular endothelial growth factor A increased in the hippocampus,while occludin and claudin-5 expression levels decreased.Co-expression of GP Ⅰa-Ⅱ integrin and type Ⅳ collagen and the number of apoptotic cells increased,whereas behavioral performance was markedly impaired.After treatment with anti-vascular endothelial growth factor receptor 2 antibody,occludin and claudin-5 expression recovered,while co-expression of GP Ⅰa-Ⅱ integrin and type Ⅳ collagen and the number of apoptotic cells decreased.Furthermore,behavioral performance improved notably.Our findings suggest that increased vascular endothelial growth factor A levels promote platelet adhesion and contribute to early brain injury after subarachnoid hemorrhage.This study was approved by the Biomedical Ethics Committee,Medical College of Xi’an Jiaotong University,China in December 2015.

关键词： nerve regeneration vascular endothelial growth factor A vascular endothelial growth factor receptor 2 subarachnoid hemorrhage brain injuries platelet adhesion collagen blood-brain barrier neural regeneration

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Spontaneous retroperitoneal hemorrhage after hemodialysis involving anticoagulant agents

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2012年第5期13卷 408-412页

作者： Wen-xing FAN Zheng-xu DENG Fang LIU Rong-bo LIU Ling HE Bogati AMRIT Li ZANG Jing-wen LI Xian-rong LIU Song-min HUANG Ping FU Department of Nephrology West China HospitalSichuan UniversityChengdu 610041China Department of Radiology West China Hospital Sichuan University Chengdu 610041China

In this paper, we described the symptoms and treatment of a patient with diabetic nephropathy accom- panied by spontaneous retroperitoneal hemorrhage after hemodialysis. An elderly female patient with diabetic neph- ropathy presented with severe pain, numbness, and an increasing swelling in the left hip and left thigh after six ses- sions of hemodialysis involving the use of an antiplatelet drug and an anticoagulant agent. Her hemoglobin decreased to 46 g/L. An abdominal ultrasound showed a hematoma in the left retroperitoneal space, and computed tomography (CT) findings revealed a 6 cm×8 cm×10 cm hematoma in the left psoas muscle. After aggressive supportive therapy [the administration of packed red blood cell transfusion, carbazochrome sodium sulfonate injection, and continuous venovenous hemofiltration (CVVH)], the patient's vital signs stabilized and her hemoglobin increased to 86 g/L. Repeat CT showed that the hematoma had been partially absorbed after two weeks. Eventually, the patient was discharged with stable vital signs. Physicians should be aware of the possibility of spontaneous retroperitoneal hemorrhage, particularly in patients with diabetic nephropathy undergoing hemodialysis involving the use of anticoagulant agents.

关键词： Spontaneous retroperitoneal hemorrhage Diabetic nephropathy Hemodialysis Nadroparin calcium

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